Correspondence

Objective: Even today there is no effective drug therapy to prevent neuronal loss after brain stroke. The objective of this research was to study effects of the mitochondrial K-ATP (MAK) channel regulators on neuronal cell population and neurological function after ischemia reperfusion in the rat. Methodology: Rats were temporarily subjected to four vessels occlusion for 15 minutes followed by 24 hours reperfusion with or without MAK channel regulators. Results: The normal cell count of neuronal population significantly increased in the K-ATP channel opener (diazoxide) treated ischemia-reperfusion group compared with the control group. Cell count and neurological function scores were dose dependent to MAK channel regulators in vivo. Conclusions: Our results showed that diazoxide treatment leads to better preservation of cortical neurons in rat